The concept of diabetic polyneuropathy encompasses disturbances of the peripheral sensory-motor and autonomous nervous system that manifest themselves by various clinical phenomena. In accordance with this definition, these syndromes are considered to be caused by the diabetic disturbances of the metabolism, the pathogenesis of which, however, is not clear, and which assumes individually varying forms of progress. Accordingly, disturbances of the blood supply by way of the vasa nervorum (microangiopathy) as well as primary disturbances of the metabolism of the nerves and of Schwann cells are assumed to be due to hypoglycemia. Pathological changes of the properties of the membranes, in particular of the neuraxon and/or disturbances of axonal transport and of transmission of signals, are considered to be the cause of the degeneration of the mechanism for the transmission of stimuli. Accordingly, therapeutic formulations represent, on the one hand, attempts to restore the metabolic derailment in the membranes by treating the underlying diabetes, and, on the other hand, attempts to eliminate membrane damage by the substitution of membrane-specific substances, such as myoinositol or gangliosides. The results of a causal therapy depend, however, not only on the formulation of the therapy, but also on the stage of the neuropathy. Especially favorable results are expected prophylactically during an early stage of the disease. As soon as structural defects of considerable extent are present, the beneficial effects of therapeutic formulae become dubious and without any clinical relevance, in-as-much as the neurons+ regenerative capability is limited, and the beneficial effects become futile in cases of advanced polyneuropathy.
Investigations of recent years have demonstrated that, after the onset of diabetes, a decrease in peripheral conduction velocity occurs when the diabetes was handled poorly. In the case of patients with disturbances of the velocity of the conduction of sensory-motor nerves or of autonomous functions, it was possible to achieve an improvement by an optimal adjustment of the metabolism. The optimalization of the metabolic condition is considered the essential basis of treatment of any form of diabetic polyneuropathy. The restoration of normal functions is, however, rarely possible and even less possible when the polyneuropathy is in an advanced state.
The findings concerning pathological changes of the systems of stimulus-conduction in diabetes, as presented herein, are comparable, as to their clinical manifestations, to numerous other neuropathies whose genesis derives from pathological changes of the nerve cells, in particular of the axon, and which reduce the velocity of stimulus conduction. Neuropathies of this type are, e.g., diabetogenic neuropathy, funicular myelosis, carcinogenic neuropathy, alcoholic polyneuropathy, neuropathies after long-term cytostatic therapy, dysglobulinemic neuropathy, myelo-optical neuropathy, encephalitis periaxialis concentrica, subacute sclerosing panencephalitis, as well as presbyophrenic cerebral dysfunctions, such as Alzheimer's disease.